GASTROENTEROLOGY Ppt Powerpoint Presentation slides-Medical Slideshow 1966 1971 Resident in Internal Medicine and Gastroenterology, Department of

GASTROENTEROLOGY

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Slide 1 :

GASTROENTEROLOGY

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OBJECTIVES Upon completion, the student will be able to: Describe the incidence, morbidity and mortality of gastrointestinal emergencies. Identify the risk factors most predisposing to gastrointestinal emergencies. Discuss the anatomy and physiology of the gastrointestinal system. Discuss the pathophysiology of abdominal inflammation and its relationship to acute pain.

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OBJECTIVES Define somatic, visceral, and referred pain as they relate to gastroenterology. Differentiate between hemorrhagic and nonhemorrhagic abdominal pain. Discuss the signs and symptoms and differentiate between local, general, and peritoneal inflammation relative to acute abdominal pain. Describe the questioning technique and specific questions when gathering a focused history in patient with abdominal pain.

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OBJECTIVES Describe the technique for performing a comprehensive physician examination on a patient complaining of abdominal pain. Discuss the pathophysiology, assessment findings, and management of the following gastroenterological problems: a) Upper gastrointestinal bleeding b) Lower gastrointestinal bleeding c) Acute gastroenteritis d) Colitis

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OBJECTIVES e) Gastroenteritis f) Diverticulitis g) Appendicitis h) Ulcer disease i) Bowel obstruction j) Crohn’s disease k) Pancreatitis l) Esophageal varices

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OBJECTIVES m) Hemorrhoids n) Cholecystitis o) Acute hepatitis Differentiate between gastrointestinal emergencies based on assessment findings. Given several scenarios involving patients with abdominal pain and symptoms, provide the appropriate assessment, treatment, and transport.

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Introduction Account for 500,000 emergency visits yearly 300,000 are due to GI bleeds Will increase because of an aging population Usually result from an underlying pathologic process that is predictable by risk factors: a) excessive alcohol consumption b) excessive smoking c) increased stress d) ingestion of caustic substances e) poor bowel habits

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General Pathophysiology Pain is the hallmark of the acute abdominal emergency. Three main classifications of abdominal pain: 1) Visceral 2) Somatic 3) Referred

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Visceral Pain Originates in the walls of hollow organs, In the capsules of solid organs, Or in the visceral peritoneum Three separate mechanisms can produce this pain: 1) Inflammation 2) Distention (being stretched out or inflated) 3) Ischemia (inadequate blood flow)

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Visceral Pain All transmit a pain signal from visceral afferent neural fibers back to the spinal column Pain is usually not localized to any one specific area Described as very vague or poorly localized, dull or crampy Body responds through sympathetic stimulation causing N/V, diaphoresis and tachycardia

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Somatic Pain Sharp type of pain that travels along definite neural routes (determined by the dermatomes) to the spinal column This pain is usually associated with perforations or ruptures of hollow organs Cause can be bacterial (ruptured appendix or gall bladder) or chemical (perforated ulcer or inflamed pancreas-leakage of acidic juices) Resulting peritonitis can lead to sepsis, and death

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Referred Pain Originates in a region other than where it is felt. Many neural pathways from various organs pass through or over regions where the organ was formed during embryonic development. Example: inflammation or injury of the diaphragm will have a referred pain in their necks or shoulders. Example: dissecting abdominal aortic aneurysm produces pain felt between the shoulder blades

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General Assessment Similar to a trauma assessment with an expanded history. Remember scene safety and BSI Observe the scene for clues and/or potential evidence of your pt’s problem: meds, alcohol, ashtrays, emesis buckets, etc..

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Scene-Size Up and Initial Assessment Determine if medical or traumatic cause If trauma remember C-spine ABC’s as always: With most medical patients, you can check responsiveness and airway by asking the patient his name and chief complaint.

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History and Physical History: including SAMPLE Then move on to History of Present Illness

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History of Present Illness OPQRST-ASPN Onset: when did the pain start, was it sudden or gradual? Provocation/Palliation: makes the pain worse or better? Quality: dull, sharp, constant? Region/radiation: pain travel? Severity: scale 1-10 Time: when and how long? Associated Symptoms Pertinent Negatives

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Physical Examination Patient’s general appearance and posture/position Complete set of vital signs Visually inspect the abdomen before palpation (distention, discoloration) Cullen’s Sign: periumbilical ecchymosis Grey-Turners Sign: ecchymosis in the flank Remove clothing as necessary Auscultation and percussion are difficult techniques in a noisy environment

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Physical Examination Palpation can give you a large amount of information: Can define the area of pain and identify the associated organs Palpate the area of discomfort last Palpation should be done with gentle pressure, feeling for: Muscle tension or its absence Masses, pulsation, tenderness

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General Treatment Once assessment, focused history and exam have been completed you now will make treatment and transport decisions. Monitor ABC’s, high-flow O2, IV access, cardiac monitor Transport in position of comfort Provide emotional reassurance The use of analgesics could limit further evaluation NOTE: persistent abdominal pain lasting longer than 6 hours is considered a surgical emergency

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Specific Illnesses Broken down into two broad categories: Upper Gastrointestinal Diseases Lower Gastrointestinal Diseases Upper GI consists of: mouth, esophagus, stomach, and duodenum Lower GI consists of: remainder of small intestine and the large intestine

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Upper GI Bleeding Bleeding within the GI tract proximal to the ligament of Treitz This ligament supports the duodenojejunal junction Accounts for 300,000 hospitalizations yearly Mortality of 10%, reasons: Increasing age of population with associated medical problems Over-the-counter treatments, until problem becomes severe

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Upper GI Bleeding Six major identifiable causes of upper GI bleed: Peptic ulcer disease Gastritis Variceal rupture Mallory-Weiss syndrome (esophageal laceration, usually secondary to vomiting) Esophagitis Duodenitis

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General Presentation Complain of some type of abdominal discomfort ranging from a vague burning sensation to an upset stomach, gas pain, or tearing pain in the upper quadrants N/V If bleeding is in the upper GI, pt. may have Hematemesis (bloody vomitus) Bleeding passes in to the lower GI tract, pt. may have Melena (tarry, foul smelling stool..partially digested blood) Bleeding can be light or life-threatening

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General Presentation Part of your assessment should include the “tilt test” (orthostatic hypotension: 10-mmHg change in BP or 20-bpm change in HR when pt. goes from supine to standing) If available the “hematocrit” could be normal in early stages but will definitely drop in the latter stages Other general complaints include: malaise, syncopal & near-syncopal, tachycardia, and indigestion.

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General Treatment Maintain airway, oxygenation and circulatory status Lateral recumbent position or semi-Fowler’s High-flow O2 Two large bore IV’s when you suspect GI bleed Cardiac Monitor

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Esophageal Varices Swollen vein in the esophagus If they rupture mortality is 35% Cause is usually a rise in portal pressure, due to impeded circulation through the liver. This will cause a backup of blood into the left gastric vein and into the esophageal veins. This will cause the veins to dilate outward, under pressure, and as the engorgement continues, cause them to rupture

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Esophageal Varices Primary cause is the consumption of alcohol and the ingestion of caustic substances. Alcohol consumption can result in cirrhosis of the liver. This will result in fatty deposits and fibrosis in the liver obstructing portal blood flow. Caustic substances can erode the esophagus from the inside out, causing hemorrhage of a vessel.

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Esophageal Varices Patients usually present initially with painless bleeding and signs of hemodynamic instability. May complain of hematemesis with bright red blood, dysphagia, and a burning or tearing sensation as the varices continue to bleed. Clotting time increases because the high portal pressure backs up blood into the spleen, destroying platelets. Classic signs of shock are common

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Esophageal Varices Treatment should focus on aggressive airway management (suction!), intravenous fluid resuscitation, placing pt. in the shock position, and rapidly transporting to the ED. ED management may include the use of a Sengstaken-Blakemore tube to tamponade the bleed, endoscopic cauterization, or sclerotherapy (injection of a thrombus-forming drug into the vein itself)

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Acute Gastroenteritis Inflammation of the stomach and intestines with associated sudden onset of vomiting and/or diarrhea. Affects 3-5 million people yearly (worldwide). 20% of all hospitalized patients The inflammation causes hemorrhage and erosion of the mucosal and submucosal layers of the GI tract

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Acute Gastroenteritis Also can damage the villi inside the intestine, which absorb water and nutrients. The water will now move through the bowel at an increased rate. Dehydration secondary to diarrhea is a common cause of death. Volume replacement is the major prehospital intervention to minimize hypovolemia.

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Acute Gastroenteritis Alcohol and tobacco abusers are at a high risk for gastritis and gastroenteritis. Also nonsteroidal anti-inflammatory drugs such as aspirin can lead to acute gastritis Alcohol and tobacco have the same effect on the mucosa as aspirin (breakdown the mucosal surfaces of stomach and GI tract) Other causes include: stress, chemotherapeutic agents and the ingestion of acidic or alkalotic agents

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Acute Gastroenteritis Infections such as salmonellosis and staphylococcus can lead to acute gastroenteritis. Onset is rapid and severe. Multiple problems arise: Diarrhea – leading to dehydration. Especially effects pediatric and geriatric patients. Stool may show melena or hematochezia (bright red blood from erosion of the lining of the lower GI tract

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Acute Gastroenteritis Hematemesis Fever N/V General malaise Patient may complain of widespread and diffuse abdominal pain that is not specific to any one region.

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Acute Gastroenteritis Treatment is mainly supportive and palliative. Position to decrease the risk of aspiration Oxygenation Rehydration Antiemetics: prochlorperazine (compazine) or promethazine (phenergan) Electrolyte replacement may be necessary at the hospital

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Chronic Gastroenteritis Inflammation of GI mucosa marked by long-term mucosal changes or permanent mucosal damage. Primarily due to microbial infection. Most prevalent pathogen in the US is Helicobacter pylori bacillus Others include: Escherichia coli, Klebsiella pneumoniae, Enterobacter, Campylobacter jejuni, Vibrio cholerae, Shigella, and Salmonella

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Chronic Gastroenteritis Viral pathogens include: Norwalk virus and rotavirus. Parasitic causes: protozoa Giardia lamblia, Cryptosporidium parvum, and Cyclosporidium cayetenis More common in underdeveloped countries Transmitted via the fecal-oral route or through infected food or water

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Chronic Gastroenteritis Commonly present with N/V, fever, diarrhea, abdominal pain, cramping, anorexia, lethargy and if severe, shock. The H.pylori presents with heartburn, abdominal pain, and gastric ulcers Treatment: BSI (protect against cross-contamination), monitoring ABCs and transport Medical treatment will require identification of the offending organism.

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Peptic Ulcers Erosions caused by gastric acid Can occur anywhere in the GI tract Location is based on the area of small intestine involved (ex. duodenal ulcer); gastric ulcers-only in the stomach Occurs 4 times more frequently in males Duodenal ulcers occur 2-3 times more often than gastric ulcers

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Peptic Ulcers Gastric ulcers more common in patients over 50, work in jobs requiring physical activity. Pain usually increases after eating or with a full stomach and they usually have no pain at night Duodenal ulcers are more common in patients from 25-50 who are executives or leaders under high stress; possible genetic predisposition Commonly have pain at night or whenever their stomach is empty

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Peptic Ulcers Nonsteroidal anti-inflammatory medications, acid-stimulating products, or Helicobacter pylori bacteria are the most common causes. GI mucosal lining is irritated by hydrochloric acid, and pepsin. Adding any of the above agents increases the irritation. Treatment is focused on antacid treatment and support of any complications (hemorrhage)

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Peptic Ulcers Blocked pancreatic duct can also contribute to duodenal ulcers. This duct releases an alkalotic solution in opposition to the high acid contained in chyme. Another cause is: Zollinger-Ellison Syndrome: Where an acid-secreting tumor provokes the ulcerations; condition causes stomach to secrete excess HCl acid and pepsin.

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Peptic Ulcers Findings on exam can vary: Chronic ulcers can cause a slow bleed with resulting anemia Visual inspection of the abdomen is only helpful with a significant bleed Palpation, the pain may be localized or diffuse Patients usually have relief of pain after eating or coating their GI tract with a liquid such as milk Acute, severe pain is probably due to a rupture of the ulcer

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Peptic Ulcers Depending on location the patient may have hematemesis or may have melena-colored stool N/V common Patient will appear ill with signs of hemodynamic instability Treatment is based on severity Position of comfort, psychological support Oxygenation, IV access for fluid resuscitation Pharmacological administration and rapid transport Meds include: Zantac and Pepcid (histamine blockers) and antacids, like Carafate

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Lower GI Diseases Lower GI tract consists of the jejunum and ileum of the small intestine, and the entire large intestine, rectum and the anus.

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Lower GI Bleeding Bleeding in the GI tract distal to the ligament of Treitz. Most frequently occur in conjunction with chronic disorders and anatomic changes associated with advanced age. Most common cause is diverticulosis. Other causes: colon lesions, rectal lesions, and inflammatory bowel disorders such as ulcerative colitis and Crohn’s disease

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Lower GI Bleed Assessment is identical as with upper GI bleeds Ask patient whether this is a new or old problem Frequent complaints with lower GI bleeds include cramping pain that may be described as like a muscle cramp or like gas pain, N/V, and changes in stool Melenic stool usually indicates a slow bleed Bright red blood, bleed is very large or has occurred in the distal colon

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Lower GI Bleed If in the distal colon, hemorrhoids or rectal fissures are possible causes. Physical presentation is similar to peptic ulcers Management is based on physiological status ABCs, oxygenation IV access, fluid resuscitation Position of comfort, cardiac monitor MAST if directed in local protocols

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Ulcerative Colitis An idiopathic inflammatory bowel disorder (IBD), that is, one of unknown origin. Creates a continuous length of chronic ulcers in the mucosal layer of the colon. As ulcers heal, granular tissue replaces the ulcerations, thickening the mucosa Typically involve the rectum or rectosigmoid portion of the large intestine.

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Ulcerative Colitis Usually starts in the rectum and then extends proximally into the colon. If it spreads throughout the entire colon it is called pancolitis; if limited to the rectum it is called proctitis. 10,000 new cases are diagnosed yearly. Affects patients between the ages of 20-40.

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Ulcerative Colitis Contributing factors: Psychological Allergic and other immunological Toxic Environmental Infectious Current research has found that the release of cytokines can cause an overwhelming inflammatory response in the submucosa

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Ulcerative Colitis Acute ulcerative colitis is difficult to differentiate from other causes of lower GI bleeds. Diagnosing may require hematocrits and hemoglobin results, guaiac analyses of the stool and endoscopic examinations. Severity is based on the extent of the current inflammation in the colon. Severe presentations usually involve the entire colon, instead of one segment

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Ulcerative Colitis Presents as a recurrent disorder with occasional bloody diarrhea or stool containing mucus. Colicky abdominal pain (cramping) N/V Fever Weight loss Cramping is usually isolated to the lower quadrants Typically appear restless due to discomfort

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Ulcerative Colitis Typically are not hemodynamically unstable More severe cases may present with bloody diarrhea and intense colicky abdominal pain. Electrolyte derangements due to fluid loss through the colon Ischemic damage to the colon itself Eventually perforation of the bowel These patients will present with S&S of hypovolemic shock

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Ulcerative Colitis Management is based on physiological status. If presenting with shock, treat as such. Additional management may include antiemetics and antispasmodic medications. Transport for diagnostic evaluation

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Crohn’s Disease The other idiopathic inflammatory bowel disorder in humans. More common in the Western Hemisphere, 20,000-30,000 new cases annually in the U.S. Tends to run in families, most prevalent in white females, those under frequent stress, and in the Jewish population. Can occur anywhere from the mouth to the rectum

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Crohn’s Disease 35-45% of less severe cases occur in the small intestine 40% involve the colon Severe cases may involve any portion of the GI tract, causing a variety of problems ranging from diarrhea to intestinal and perianal abscesses and fistulas Complete intestinal obstruction can also occur Significant lower bleeding is rare.

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Crohn’s Disease It damages the innermost layer of the tissue the mucosa. Affected section of intestinal wall eventually becomes rubbery and nondistendable due to hypertrophy and fibrosis of the muscles underlying the submucosa. This will decrease the intestine’s internal diameter, resulting in fissures (incomplete tears) in the mucosa

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Crohn’s Disease If a tear extends into the blood vessels in the submucosal layer, small bleeds result. Clinical presentations vary drastically as the disease progresses, and prehospital diagnosis is virtually impossible

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Signs & Symptoms GI bleeding Recent weight loss Intermittent abdominal cramping/pain N/V Diarrhea Fever

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Crohn’s Disease Flareup is usually rapid, requiring a visit to the doctor Abdominal pain cannot be localized to any specific quadrant Physical exam is also nonspecific, and nonlocalized, with diffuse tenderness the most commonly found sign. Prehospital treatment is palliative because the patient is generally hemodynamically stable

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Crohn’s Disease Management depends on the patient’s physiological status Additional management may include antiemetics and antispasmodic medications

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Diverticulitis Relatively common complication of diverticulosis. Diverticulosis is a condition characterized by the presence in the intestine of diverticula, small outpouchings of mucosal and submucosal tissue that push through the outermost layer of the intestine, the muscle. Diverticulitis is an inflammation of diverticula secondary to infection.

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Diverticulitis It is symptomatic, patients complain of lower left-sided pain (located in sigmoid colon) Exam and testing will show fever and an increased WBC count Pathogenesis of a diverticulum is twofold: Stool passes sluggishly through the colon, a condition associated with the relatively low fiber diets common in developed countries. Colon responds with muscle spasms to move the fecal material forward

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Diverticulitis The outermost layer of colon tissue is made up of fibrous bands of muscle wrapped around one another. The muscles (teniae coli) become weakened with age, and the increased pressure of muscle spasms can cause the inner layers of tissue, the mucosa and submucosa, to herniate through the openings, forming diverticula. The diverticula then trap small amounts of fecal material, including sunflower seeds, popcorn fragments, okra seeds, sesame seeds etc.. the trapped feces can allow bacteria to grow and result in an infection.

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Diverticulitis When diverticula become inflamed the result is diverticulitis Complications include possible hemorrhage, larger perforations of the colon in which the fecal matter is spilled into the peritoneal cavity and cause peritonitis. Most common presentation is colicky pain associated with low grade fever, N/V, tenderness upon palpation

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Diverticulitis If they begin to bleed significantly the presentation is similar with any serious lower GI bleed (sympathetic response) Bleeding diverticula can also result in bright red and bloody feces (hematochezia) Prehospital treatment is mainly supportive, treat for shock as necessary Antiemetics (Phenergan or Vistaril) for comfort In hospital: antibiotic therapy, endoscopy, radiological tests

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Hemorrhoids Small masses of swollen veins that occur in the anus (external) or rectum (internal) Frequently develop during the fourth decade of life. Most are idiopathic, but can result from pregnancy or portal hypertension. External hemorrhoids often result from lifting a heavy object.

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Hemorrhoids Other causes include: Straining at defecation Diet low in fiber Internal hemorrhoids most often involve the inferior hemorrhoidal plexus and vasculature. Commonly bleed during defecation and then thrombose into closed state again External hemorrhoids result from a thrombosis of a vein, often following lifting or straining

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Hemorrhoids External hemorrhoids cause bright red blood with bowel movement. Vessels can erode from increased venous pressure, causing free bleeding and high risk for infection. Patients usually call because of bright red bleeding and pain on defecation. Patients are typically hemodynamically stable Treatment is based on patient’s condition

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Bowel Obstruction Blockages of the hollow space, or lumen, within the small and large intestines Can be either partial or complete Can be catastrophic if not rapidly diagnosed and treated Many different causes. Four most frequent are: Hernia: protrusion or organ through its protective sheath Intussusception: part of intestine slips into the part just distal to itself Volvulus: twisting of the intestine Adhesions: union of normally sep. tissue by a fibrous band of new tissue

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Bowel Obstruction Other causes include: foreign bodies, gallstones, tumors, adhesions from previous abdominal surgery, and bowel infarction. Most common location is the small intestine, due to its smaller diameter and its greater length, flexibility, and mobility Obstruction may be chronic, as with tumor growth or adhesion progression Or acute as with foreign body obstruction

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Bowel Obstruction Chronic obstruction usually results in a decreased appetite, fever, malaise, N/V, weight loss, or if rupture occurs (peritonitis). Acute-onset pain may follow ingestion of a foreign body. Pain may also be due to strangulation, possibly leading to infarction. Patients frequently vomit, vomitus often containing a significant amount of bile.

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Bowel Obstruction Patients present with diffuse visceral pain, usually poorly localized to any one specific location. Hemodynamically unstable due to necrosis of an organ, S&S of shock may be present Abdominal distention may be obvious (free air) from a rupture of the strangulated segment Palpation will reveal tenderness Treatment is based on physiological status

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Accessory Organ Disease These include: Liver Gallbladder Pancreas Vermiform Appendix

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Appendicitis Inflammation of the vermiform appendix Occurs in approximately 10-20% of the population in the US Most common in young adults Acute appendicitis is the most common surgical emergency you will encounter in the field There are no particular risk factors

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Appendicitis Appendix serves no anatomic or physiologic function, lymphoid tissue It can become inflamed and rupture if left untreated, resulting in peritonitis Pathogenesis: most often due to obstruction of the appendiceal lumen by fecal material. Results in inflamed lymphoid tissue and leads to bacterial or viral infection

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Appendicitis The inflammation also causes the internal diameter to expand, blocking the artery, causing infarction and necrosis. Leading to rupture. Mild or early appendicitis causes diffuse, colicky pain associated with N/V, and low-grade fever. Pain is initially located in the periumbilical region Patient also loses their appetite Continued dilation causes pain to localize in the right lower quadrant

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Appendicitis Once the appendix ruptures the pain becomes diffuse due to development of peritonitis Physical exam shows a patient in discomfort. Abdominal exam reveals tenderness or guarding around the umbilicus or RLQ Common site of pain is McBurney’s point Prehospital care is based on the hemodynamic state of the patient

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Cholecystitis Inflammation of the gallbladder. Cholelithiasis (formation of gall stones), causing 90% of cholecystitis in the US 1 million new cases annually. Two types of gallstones: Cholesterol-based Bilirubin-based

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Cholecystitis Cholesterol-based stones are far more common and are associated with a specific risk profile: obese, middle-aged women with more than one biological child Definitive treatment of acute cholecystitis include antibiotic therapy, laparoscopic surgery, lithotripsy (ultrasound) and surgery.

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Cholecystitis Gallstones occur because of calculi build up lodging in the common bile duct. When the movement of bile is obstructed gallbladder inflammation and irritation result. Over time blood flow to the local epithelium will be reduced. Other causes of cholecystitis include: Acalculus cholecystitis (no stones) Chronic inflamation: caused by bacterial infection

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Cholecystitis Acalculus cholecystitis usually results from burns, sepsis,diabetes, and multiple organ failure. Inflamed gallbladder usually causes an acute attack of upper right quadrant abdominal pain, with referred pain in the right shoulder. If gallstones are lodged in the cystic duct, the pain may be colicky, due to expansion and contraction.

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Cholecystitis The pain occurs after a meal that is high in fat content because of the secondary release of bile from the gallbladder. Palpation may reveal either diffuse right-sided tenderness or point tenderness under the right costal margin, a positive Murphy’s sign. Prehospital treatment is mainly palliative. Position of comfort, maintain ABCs, establish IV Pain medication: meperidine (demerol) & butorphanol (stadol)

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Pancreatitis Inflammation of the pancreas Four main categories, based on cause: Metabolic Mechanical Vascular Infectious

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Pancreatitis Metabolic causes, specifically alcoholism, account for 80% of all cases Mechanical obstructions caused by gallstones or elevated serum lipids account for another 9% Vascular injuries caused by thromboembolisms or shock, along with infectious diseases, account for the remaining 11% Mortality (30-40%) is due sepsis and shock.

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Pancreatitis Acute pancreatitis caused by gallstones that obstruct the pancreatic duct. Results in backups of digestive enzymes, causing inflammation of the pancreas and edema, reduction of blood flow, ischemia and acinar destruction. Acinar tissue destruction causes a second form of pancreatitis, chronic pancreatitis.

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Pancreatitis Acinar tissue destruction commonly occurs due to chronic alcohol intake, drug toxicity, ischemia, or infectious diseases. Pain can be localized to the left upper quadrant or may radiate to the back or the epigastric region. Most patients experience nausea followed by uncontrolled vomiting and retching that can further aggravate the hemorrhage.

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Pancreatitis Patient will appear acutely ill with diaphoresis, tachycardia, and possible hypotension. Prehospital treatment is supportive and aimed at maintaining the ABCs Establish IVs Definitive treatment involves gastric intubation and suctioning for emesis control, diagnostic peritoneal lavage, antibiotic therapy, fluid resuscitation, and surgery to remove the blockage.

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Hepatitis Involves any injury to hepatocytes associated with an inflammation or infection. Five viruses: A, B, C, D, and E Alcoholic hepatitis, arises from alcoholic cirrhosis, rather than an infectious agent. Factors that increase the risk of contracting hepatitis include: unsanitary living conditions, poor personal hygiene that invites oral-fecal transmission, exposure to blood borne pathogens, and chronic alcohol intake.

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Hepatitis Any of the viral pathogens, alcoholic exposure, or trauma can injure the hepatocytes, causing inflammation and, possibly, chronic liver disease. Whatever the cause, results are similar: enlargement and hypertrophy, fatty changes, loss of architecture, and appearance of lesions and spontaneous hemorrhages Symptoms range from mild to liver failure and death

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Hepatitis Hepatitis A is probably the best known. Commonly referred to as infectious hepatitis. Spreads by oral-fecal route Disease is self-limiting Lasting between 2-8 weeks. Low mortality rate

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Hepatitis Hepatitis B, known as “serum hepatitis” Blood borne pathogen that can stay active in bodily fluids outside the body for days. 310 million carriers worldwide, HBV is an epidemic. Effects may be minimal, but can range to severe liver ischemia and necrosis

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Hepatitis Hepatitis C caused by the pathogen most commonly responsible for spreading hepatitis through blood transfusions Marked by chronic and often debilitating damage to the liver.

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Hepatitis Hepatitis D, less common disorder because its pathogen is dormant until activated by HBV. Hepatitis E is a waterborne infection that has caused epidemics in Africa, Mexico, and other third-world nations. Mortality rate for pregnant women is high.

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Hepatitis Commonly present with symptoms relative to the severity of their disease. Complain of URQ abdominal tenderness, not relieved by antacids, food, or positioning. May lose their appetite and become anorexic, usually losing weight. Decrease in bile production changes their stool to a clay color, and increased bilirubin retention causes jaundice, yellow coloring of the skin, and scleral icterus, yellowing of the white of the eyes

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Hepatitis Other signs and symptoms include severe N/V, general malaise, photophobia, pharyngitis, and coughing Exam will reveal a sick patient, possibly with a jaundiced appearance. Pain may present in URQ or the right shoulder Fever may be secondary to infection or to tissue necrosis

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Hepatitis Treatment is palliative. Secure ABCs Establish IV Antiemetic administration Definitive treatment involves antiviral and anti-inflammatory medications and symptomatic treatment

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Acalculus cholecystitis usually results from burns, sepsis,diabetes, and multiple organ failure. In more Acalculus cholecystitis usually results from burns, sepsis,diabetes, and multiple organ failure. Inflamed gallbladder usually causes an acute attack of ... less

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